Iranian Journal of Toxicology
Volume:17 Issue: 4, Oct 2023

Antiaris africana has been shown to protect against several neurotoxins. This study investigated the neuroprotective effect of the ethylacetate fraction of A. africana (EFA) against sodium azide neurotocity (NaN3).

The corpora striata from the brains of 30 male Wistar rats were removed and incubated with varying concentrations of EFA in the presence or absence of NaN3. The protective effect of EFA was assessed by measuring the concentrations and activities of different mitochondrial respiratory enzymes (MRE) (NADH cytochrome C reductase, NADH succinate dehydrogenase, succinate cytochrome C reductase), neurotransmitters (acetylcholinesterase), reduced glutathione, malondialdehyde, protein carbonyl, lactate dehydrogenase, and monoamine oxidase.

The results indicated that NaN3 inhibited the activities of the MRE as compared to that of the controls (P<0.05).  It released lactate dehydrogenase from the striata, increased the activity of acetylcholinesterase, caused oxidative stress, and increased monoamine oxidase activity as compared to those of the control (P<0.05). The observed toxicity effect of NaN3 was prevented by all of the administered concentrations of EFA.

Our current findings support the fact that A. africana fraction was able to protect the mitochondrial enzymes involved in the respiratory chain, improve the redox status and prevent leakage of enzymes from the brain tissue, which demonstrated the efficacy of A. africana in preventing the toxic effect of NaN3 on rat brain cells and tissue.

Nowadays, due to the increasing problems of microbial resistance, scientists are searching for the safest and most effective way to fight them. The colloidal silver (Ag) and titanium dioxide (TiO2) nanoparticles can effectively fight against many bacterial microorganisms. Therefore, the purpose of this study was to investigate the antibacterial and cytotoxic properties of Ag and TiO2 nanoparticles, against Shigella dysenteriae and Staphylococcus aureus.

In this study, Ag and TiO2 nanoparticles were synthesized, and the minimum inhibitory and bactericidal concentrations (MIC & MBC) were determined. In addition, the cytotoxicity of these agents was evaluated on Hu02 fibroblast cell line.

We found that the MIC and MBC for Ag and TiO2 nanoparticles were similar (12.5 µg/ml) against S. aureus, while the MIC’s for Ag and TiO2 against S. dysenteriae were found to be 12.5 and 25 µg/ml. In addition, the MBC’s for Ag and TiO2 against S. dysenteriae were 25 and 50 µg/ml. Based on the cytotoxicity tests, the cell viability percentage after 48 hours of exposure to TiO2 was higher than that of Ag (0.025 µg/ml).

The Ag and TiO2 nanoparticles demonstrated good antibacterial properties while they had low toxicity against the Hu02 fibroblast cell line.

Autism, a neurodevelopmental disorder that manifests early in childhood but the pathogenic risks are controversial, and some environmental factors are thought to be involved. The association between toxic heavy metals and autism is currently a subject of research, and studies are underway on the role of toxic heavy metals in Egypt, focusing on the social, cultural, and environmental aspects. We investigated the aluminum, cadmium and lead levels in the hair and blood samples of Egyptian autistic children.

This study was conducted between July 2021 and December 2022 on 32 children with diagnosed autism, aged three to 13 years old, whom were compared with 30 age- and gender-matched children (normal controls). These children were subjected to childhood autism rating scale (CARS), and IQ tests. Also, the aluminum, cadmium, and lead levels were measured in their hair and blood samples for further statistical analyses.

The autistic children had significantly higher levels of aluminum, lead, and cadmium in the hair samples compared to those of the controls. Also, the blood levels of aluminum and cadmium were significantly higher in the autistic children. Those with severe autism had a higher level of hair aluminum compared to those with mild autism. We found positive correlations among the CARS data versus hair aluminum and blood cadmium levels. The regression analyses on blood cadmium levels were also predictive of CARS.

The study findings suggest a likely role for the three heavy metals as being the potential environmental triggers of autism in children.

Environmental pollutants, such as plastic-derived substances Bisphenol-A and Di-butyl phthalate have been linked to an increase in the occurrence of human health hazards, including dysmetabolic syndrome, i.e., insulin resistance, and organ toxicity. In this syndrome, concurrent risk factors can give rise to cardiovascular disease, stroke, and type 2 diabetes.  This study aimed to investigate the toxic effects of certain plastic compounds against kidneys and liver, and the potential protective role of rutin in rat. Rutin is a natural anti-inflammatory supplement that improves blood circulation and metabolic functions, lowers cholesterol and reduce arthritis pain.

Eighteen rats were divided randomly into three groups of six each and were treated for 28 days as follows: 1) Control (0.1% DMSO); 2) Bisphenol-A and Dibutyl phthalate, and 3) Bisphenol-A, Dibutyl phthalate and rutin. At the completion of the experimental period, the rats’ hepatic and renal toxicity biomarkers, redox status and lipid profile were measured.

Based the experimental findings, the toxicity of plastic substances increased in gamma-glutamyl transferase, urea, renal MDA and significant reductions in SOD and CAT activities, compared to those of the controls. The total plasma cholesterol and low-density lipoprotein (LDL) levels increased. The hepatic total cholesterol, LDL, FFA, TG levels increased. The HDL decreased while the total cholesterol, TG and LDL levels increased in the kidney. However, these biochemical alterations improved significantly by administering rutin supplement to the rats that were pretreated with the plastic compounds.

Flavonoid, rutin, demonstrated hepato-renal protective effect against the toxic effects of plastic compounds.

Breast cancer is a common human neoplasia in women. Species of the Lamiaceae plant have been found to exert in vitro anti-proliferative activity on breast cancer cells. The aim of this study was to evaluate the cytotoxic effect of the extracts of ten species from the Lamiaceae family on a breast cancer cell line. We also examined the selective indices of the fractions and essential oil of the most effective extract.

The plant species were harvested, dried and authenticated. The hydro-alcoholic extract of each plant was examined for its cytotoxicity on the breast cancer cell line (MCF-7) using MTT assay. The n-Hexane, chloroform and ethyl acetate fractions were prepared from Nepeta crispa extract. Hydro-distillation method was used to isolate the Nepeta crispa’s essential oil. The essential oil and the fractions were examined in vitro for the cytotoxic effects against both HEK293 and MCF-7 cell lines.

The Nepeta crispa extract exhibited significant cytotoxic activity on MCF-7 (IC50 = 59 ±3.4μg/mL) compared to other extracts. The n-hexane fraction of Nepeta crispa demonstrated the highest cytotoxicity (IC50 = 65.47 ±4.3μg/mL) among other fractions. The essential oil exhibited concentration-dependent inhibition against the growth of cancer cells, and showed the most inhibitory effect against MCF-7 cells (IC50 = 18.15 ±2.7μg/mL) with a selectivity index of 9.69.

Based on the results, the n-hexane fraction and essential oil of Nepeta crispa may be the potential sources of biologically active components to develop novel drugs for breast cancer treatment.

Aflatoxin B1 (AFB1), one of the main types of aflatoxins, is the most dangerous and prevalent. Due to its side effect to the liver, AFB1 has been linked to an increased risk of hepatocellular carcinoma. This study's goal was to assess how the nanoparticles of lactoferrin (LF) protects rat liver from the toxicity caused by aflatoxin B1, as an antioxidant and anti-inflammatory compound.

Forty adult male Wistar rats (140-200g each) were divided into four groups of ten each: 1) A group of healthy animals; 2) healthy rats treated with PEE (50 mg/kg/day); 3) rats given Aflatoxin B1 (40 mg/kg/day) orally for six weeks; 4) rats injected with LF-NPs for six weeks after being intoxicated with AFB1.

The results showed that LF was successful in reducing AFB1-induced hepatotoxicity after six weeks of treatment. This was demonstrated by a significant decline in the serum ALAT, ASAT, GGT, ALP, TNF-α, IL-1β, CD4 and AFP levels, and hepatic MDA, NO, and DNA fragmentation.  Also, significant increase in the serum total protein and albumin, hepatic GSH, SOD, and CAT values were investigated. These effects were consistent with the structural restoration of the histological status of the liver.

It is possible to draw the conclusion that LF-NPs have been highly effective in reducing the oxidative stress caused by AFB1 and protecting the liver from its harmful effects. LF-NPs may be thought of as an exciting candidate for safeguarding the liver from the adverse effects of AFB1.

Oral ingestion of lead in drinking water represents the most common route of human and animal exposure, especially in the developing nations. Unlike other internal organs, research on the effects of lead on gastrointestinal tract remains limited. This study explored the alterations in faecal fatty acid composition, gastrointestinal and hepatic histologies and redox status, following chronic, 90-day exposure of rats to lead acetate (PbA). We also investigated the protective effects of rutin and melatonin against lead toxicity in rats.

Fifty male Wistar rats were randomly divided into five groups of 10 (A-E) and were assigned as follows: A: Control; B: 1% PbA in drinking water; C: PbA+rutin (50 mg/kg); D: PbA+melatonin (25 mg/kg) and E: PbA+rutin+melatonin. The faecal fatty acid profiles were quantified by methylation and gas chromatography-flame ion detection. We also evaluated the oxidative stress and antioxidant markers for the stomach, liver, and guts, and their histopathological alterations.

Exposure to PbA caused remarkable elevations of the faecal fats, such as undecylic, lauric, tridecylic, myristic, and palmitic acids, compared to the controls and rats in group C. The administration of rutin and/or melatonin ameliorated the PbA-induced increases in the hydrogen peroxide and malondialdehyde contents. Rutin and melatonin improved the levels of thiol, and reduced the glutathione, glutathione S-transferase and superoxide dismutase activities.

The findings suggest that rutin alone or combined with melatonin protects against PbA-induced disruption of the liver and gastrointestinal tract integrity via modulation of intestinal total lipids in cells and redox imbalances.

Recently, advances have emerged in medicine and pharmacotherapeutics, providing novel treatments for tuberculosis (TB). It is noteworthy that long-term drug consumption for TB treatment often leads to hepatotoxicity, which can have serious or even fatal side effects. Thus, many studies have focused on the assessment of the hepatoprotective effects of betaine, a glycine derivative. This study aimed at evaluating the effects of betaine to explore the underlying biochemical mechanisms of hepatotoxicity in rats, using combined isoniazid (INH) and rifampicin (RMP).

We used an animal model to induce hepatotoxicity with combined INH-RMP and to determine the protective effects of betaine at three doses of 125, 250 and 500 mg/kg.

Treatment with INH and RMP led to a significant upregulation of hepatic damage markers, along with marked alteration in the histopathological lesions. The results after the use of betaine were found to be satisfactory at 500 mg/kg comparable to silymarin (200mg/kg). The hepatotoxicity was also found to be associated with generation of reactive oxygen species (ROS) and oxidative stress, indicating the deterioration of the antioxidant defense system in the liver. However, pretreatment with betaine seemed to ameliorate the INH-RMP-induced hepatotoxicity, along with marked down-regulation of oxidative stress and hepatotoxicity markers.

The study findings indicated that treatment with betaine may help alleviate the INH-RMP-induced liver pathology. This was evident by the reduced inflammation and oxidative stress via mitochondrial GSH regeneration, ROS inhibition, and protection of mitochondria complex II. Further studies are warranted to investigate the validity of these outcomes.